ArticleFrontiers in endocrinology2022
Hepatic overexpression of protein targeting to glycogen attenuates obesity and improves hyperglycemia in db/db mice.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Hyperglycemia impairs cognitive function by inducing mitochondrial damage through lactylation of LRPPRC at K223.EMBO molecular medicine · 2026Article
- Hepatic HuR modulates glucose metabolism through the C/EBPβ/PCK1 pathway.Molecular metabolism · 2026Article
- Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Protein Phosphatase 1 Regulatory Subunit 3C integrates cholesterol metabolism and isocitrate dehydrogenase in chondrocytes and neoplasia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Farrerol alleviates insulin resistance and hepatic steatosis of metabolic associated fatty liver disease by targeting PTPN1.Journal of cellular and molecular medicine · 2024Article
- The role of adipose tissue dysfunction in hepatic insulin resistance and T2D.The Journal of endocrinology · 2024Review
- Active Glycogen Synthase in the Liver Prevents High-Fat Diet-Induced Glucose Intolerance, Decreases Food Intake, and Lowers Body Weight.International journal of molecular sciences · 2023Article
- Glucose Sensing in the Hepatic Portal Vein and Its Role in Food Intake and Reward.Cellular and molecular gastroenterology and hepatology · 2023Review
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3 authors.
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Abstract
Increased liver glycogen content has been shown to reduce food intake, attenuate obesity, and improve glucose tolerance in a mouse model of high-fat diet (HFD)-induced obesity. Here we studied the contribution of liver glycogen to the regulation of obesity and glucose metabolism in a model of type 2 diabetes and obesity, namely the db/db mouse. To this end, we crossed db/db mice with animals overexpressing protein targeting to glycogen (PTG) in the liver to generate db/db mice with increased liver glycogen content (db/db-PTG). Hepatic PTG overexpression reduced food intake and fat weight and attenuated obesity and hyperglycemia in db/db mice. Db/db-PTG mice showed similar energy expenditure and physical activity to db/db mice. PTG overexpression reduced liver phosphoenolpyruvate carboxykinase (PEPCK) protein levels and repressed hepatic glucose production in db/db mice. Moreover, increased liver glycogen elevated hepatic ATP content in these animals. However, lipid metabolism was not modified by PTG overexpression. In conclusion, increased liver glycogen content ameliorates the diabetic and obesity phenotype in db/db mice.
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